This pathophysiologic argument has been supported by the findings that brief or absent labor and short or absent time in the birth canal have been associated with TTN.2, 3 It has long been hypothesized that mechanical forces of labor and delivery work to "squeeze" edema away from air-exchange surfaces of the lung into the lymphatics. More recently, studies have demonstrated that immaturity of sodium ion channel transporters in the lung epithelium may play a more significant role in the failure of pulmonary fluid reabsorption than mechanical forces.4, 5 Data from animal models show that absent labor, such as found in scheduled Cesarean sections, may lead to delivery before the normal hormonally-mediated upregulation or activation of these sodium transporters occurs and thus may explain the increased likelihood of developing TTN seen in this patient cohort.